Antimicrobial agents are useful for control of bacterial infections in food animals and man. Their prudent use in these animals is important to control any possible development and transfer of resistance between animals and man. The objective of this study was to generate quantitative information to evaluate antimicrobial usage patterns by animal species, route of administration, antimicrobial class and type of use from 1995 to 1999 in Kenya. Theses data are essential for risk analysis and planning and can be helpful in interpreting resistance surveillance data, and evaluating the effectiveness of prudent use efforts and antimicrobial resistance mitigation strategies. Data on quantities of active substance classes were collected from the official records of the Pharmacy and Poisons Board of the Ministry of Health and analysed in MS Excel 2000 program. The mean antimicrobial consumption for the 5-year period was 14 594 ± 1457 kg per year. This was distributed in the various antimicrobial classes as follows: 7975 kg (54.65%) of tetracyclines, 3103.96 kg (21.27%) of sulfonamides and 954.5 kg (6.56%) of aminoglycosides, 905 kg (6.20%) of β-lactams, 94 kg (0.64%) of quinolones, 35 kg (0.24%) of macrolides and 24 kg (0.16%) of others (tiamulin). Mean consumption per year among the various food animals was: 10 989 ± 357 kg in large animals (cattle, sheep, pigs and goats), 2906 ± 127 kg in poultry alone and 699 ± 427 kg in both large animals and poultry. These quantities represented 56.56% (8255 kg) consumption per year for parenteral use, 41.79% (6098 kg) for oral use and 1.65% (241 kg) for topical use (intramammary and eye ointments) in cattle. With respect to intended use in food producing animals, the mean consumption per year was: 13 178 kg (90.30%) for therapeutic use (ST), 4 kg (0.03%) for prophylactic treatment (PT) and 1411 ± 246 kg (9.67%) was used both for therapeutic and prophylactic purposes (GPT). The study confirmed that antimicrobials are not used for growth promotion in Kenya. There was no specific trend in the quantities of active antimicrobial classes. This study has revealed that the tetracyclines, sulfonamides and trimethoprim, nitrofurans aminoglycosides, β-lactams and the quinolones are the most commonly used drugs in food-producing animals in Kenya. Tetracyclines contributed approximately 55% of the total consumption, and there was an increasing trend in the consumption of quinolones from 1998.

The prevalence of gastrointestinal helminths was investigated by the examination of 255 faecal samples from different age groups and sexes of camels maintained in a communal grazing environment in northern Kenya between November 1992 and March 1993. In addition, 73 fresh faecal samples from anaemic camels and those with an eggs per gram (epg) count of >1000 were cultured for larval identification. The results showed that peak worm infestations occurred during and soon after the onset of rains. Female camels had significantly higher egg counts than males. Immature bulls had lower egg counts than calves which had lower egg counts than adults. More than 80% of the parasites identified were nematodes, of which Haemonchus was most frequent, followed by Trichostrongylus; relatively few of the camels were infected with Cooperia, Bunostomum, Oesophagostomum, Strongyloides and Ostertagia. The most frequent cestode was Moniezia. Eggs of Fasciola were identified in a few of the camels; this is the first report of fascioliasis in camels in Kenya.

Tetracyclines have been among the most widely used antibiotics worldwide. Plasmid-mediated tetracycline resistance among hospital strains of bacteria has continued to rise and of major concern has been the transfer of resistance to pathogenic organisms. Bacteraemia due to hospital acquired S. typhimurium has been a major cause of morbidity at Kenyatta National Hospital (KNH), hence the need to study drug susceptibility pattern of this organism. This study also characterized the tetracycline resistance genes using oligonucleotide probes. Ninety seven S. typhimurium strains isolated from patients at KNH were used. Agar dilution method was used to determine minimum inhibitory concentration (MIC). Plasmids were isolated from each strain and the different plasmid profiles were grouped by their molecular weights into 6 patterns. Out of 97, 87 (88%) strains were resistant. MIC ranged from 1 microgram/ml to 128 micrograms/ml. Genes encoding for tetracycline resistance were located on plasmids of molecular weights 65 MDa, 5.2 or both. Plasmid-encoded antimicrobial resistance is likely to spread to other pathogenic organisms, reduce our ability to treat the infection and increase the cost and duration of treatment.

Buparvaquone, a naphthoquinone with known efficacy against Theileria parva parva in cattle, was tested for activity against Theileria cervi piroplasms in both an in vitro culture system and in vivo in experimentally infected white-tailed deer. The in vitro data showed a significant decrease in the incorporation of 3H-hypoxanthine by infected red blood cells treated with buparvaquone when compared to that seen with imidocarb and chloroquine treatment. In both intact and splenectomized deer treated with buparvaquone (2.5 mg kg-1) a gradual decrease in piroplasm parasitaemia was observed following treatment. However, in the splenectomized deer, parasitaemia levels returned to near pretreatment values after approximately 2 weeks

Two groups of 6 rats each received subcutaneous injections of 2.3 mg/kg or 5.0 mg/kg of quinuronium, respectively, on two consecutive days, while 5 rats injected with physiological saline served as controls. Clinical signs of muscular tremors, jumps, enlarged and hyperemic eyeballs, lacrimation, depression and anorexia were observed following administration of quinuronium. One rat receiving 5 mg/kg died before termination of the study. When killed 48 h after the first injection, the quinuronium-treated rats had a higher liver weight/body weight ratio compared to the controls. Quinuronium resulted in hepatic centrilobular fatty degeneration, but no depletion of hepatic glutathione (GSH). The present findings suggest that glutathione depletion does not seem to be involved in quinuronium hepatotoxicity.

Two groups of 6 rats each received subcutaneous injections of 2.3 mg/kg or 5.0 mg/kg of quinuronium, respectively, on two consecutive days, while 5 rats injected with physiological saline served as controls. Clinical signs of muscular tremors, jumps, enlarged and hyperemic eyeballs, lacrimation, depression and anorexia were observed following administration of quinuronium. One rat receiving 5 mg/kg died before termination of the study. When killed 48 h after the first injection, the quinuronium-treated rats had a higher liver weight/body weight ratio compared to the controls. Quinuronium resulted in hepatic centrilobular fatty degeneration, but no depletion of hepatic glutathione (GSH). The present findings suggest that glutathione depletion does not seem to be involved in quinuronium hepatotoxicity.

Two groups of 6 rats each received subcutaneous injections of 2.3 mg/kg or 5.0 mg/kg of quinuronium, respectively, on two consecutive days, while 5 rats injected with physiological saline served as controls. Clinical signs of muscular tremors, jumps, enlarged and hyperemic eyeballs, lacrimation, depression and anorexia were observed following administration of quinuronium. One rat receiving 5 mg/kg died before termination of the study. When killed 48 h after the first injection, the quinuronium-treated rats had a higher liver weight/body weight ratio compared to the controls. Quinuronium resulted in hepatic centrilobular fatty degeneration, but no depletion of hepatic glutathione (GSH). The present findings suggest that glutathione depletion does not seem to be involved in quinuronium hepatotoxicity.

Two groups of 6 rats each received subcutaneous injections of 2.3 mg/kg or 5.0 mg/kg of quinuronium, respectively, on two consecutive days, while 5 rats injected with physiological saline served as controls. Clinical signs of muscular tremors, jumps, enlarged and hyperemic eyeballs, lacrimation, depression and anorexia were observed following administration of quinuronium. One rat receiving 5 mg/kg died before termination of the study. When killed 48 h after the first injection, the quinuronium-treated rats had a higher liver weight/body weight ratio compared to the controls. Quinuronium resulted in hepatic centrilobular fatty degeneration, but no depletion of hepatic glutathione (GSH). The present findings suggest that glutathione depletion does not seem to be involved in quinuronium hepatotoxicity.

Two groups of 6 rats each received subcutaneous injections of 2.3 mg/kg or 5.0 mg/kg of quinuronium, respectively, on two consecutive days, while 5 rats injected with physiological saline served as controls. Clinical signs of muscular tremors, jumps, enlarged and hyperemic eyeballs, lacrimation, depression and anorexia were observed following administration of quinuronium. One rat receiving 5 mg/kg died before termination of the study. When killed 48 h after the first injection, the quinuronium-treated rats had a higher liver weight/body weight ratio compared to the controls. Quinuronium resulted in hepatic centrilobular fatty degeneration, but no depletion of hepatic glutathione (GSH). The present findings suggest that glutathione depletion does not seem to be involved in quinuronium hepatotoxicity.

Two groups of 6 rats each received subcutaneous injections of 2.3 mg/kg or 5.0 mg/kg of quinuronium, respectively, on two consecutive days, while 5 rats injected with physiological saline served as controls. Clinical signs of muscular tremors, jumps, enlarged and hyperemic eyeballs, lacrimation, depression and anorexia were observed following administration of quinuronium. One rat receiving 5 mg/kg died before termination of the study. When killed 48 h after the first injection, the quinuronium-treated rats had a higher liver weight/body weight ratio compared to the controls. Quinuronium resulted in hepatic centrilobular fatty degeneration, but no depletion of hepatic glutathione (GSH). The present findings suggest that glutathione depletion does not seem to be involved in quinuronium hepatotoxicity.

Two groups of 6 rats each received subcutaneous injections of 2.3 mg/kg or 5.0 mg/kg of quinuronium, respectively, on two consecutive days, while 5 rats injected with physiological saline served as controls. Clinical signs of muscular tremors, jumps, enlarged and hyperemic eyeballs, lacrimation, depression and anorexia were observed following administration of quinuronium. One rat receiving 5 mg/kg died before termination of the study. When killed 48 h after the first injection, the quinuronium-treated rats had a higher liver weight/body weight ratio compared to the controls. Quinuronium resulted in hepatic centrilobular fatty degeneration, but no depletion of hepatic glutathione (GSH). The present findings suggest that glutathione depletion does not seem to be involved in quinuronium hepatotoxicity.

Two groups of 6 rats each received subcutaneous injections of 2.3 mg/kg or 5.0 mg/kg of quinuronium, respectively, on two consecutive days, while 5 rats injected with physiological saline served as controls. Clinical signs of muscular tremors, jumps, enlarged and hyperemic eyeballs, lacrimation, depression and anorexia were observed following administration of quinuronium. One rat receiving 5 mg/kg died before termination of the study. When killed 48 h after the first injection, the quinuronium-treated rats had a higher liver weight/body weight ratio compared to the controls. Quinuronium resulted in hepatic centrilobular fatty degeneration, but no depletion of hepatic glutathione (GSH). The present findings suggest that glutathione depletion does not seem to be involved in quinuronium hepatotoxicity.

Two groups of 6 rats each received subcutaneous injections of 2.3 mg/kg or 5.0 mg/kg of quinuronium, respectively, on two consecutive days, while 5 rats injected with physiological saline served as controls. Clinical signs of muscular tremors, jumps, enlarged and hyperemic eyeballs, lacrimation, depression and anorexia were observed following administration of quinuronium. One rat receiving 5 mg/kg died before termination of the study. When killed 48 h after the first injection, the quinuronium-treated rats had a higher liver weight/body weight ratio compared to the controls. Quinuronium resulted in hepatic centrilobular fatty degeneration, but no depletion of hepatic glutathione (GSH). The present findings suggest that glutathione depletion does not seem to be involved in quinuronium hepatotoxicity.

Two groups of 6 rats each received subcutaneous injections of 2.3 mg/kg or 5.0 mg/kg of quinuronium, respectively, on two consecutive days, while 5 rats injected with physiological saline served as controls. Clinical signs of muscular tremors, jumps, enlarged and hyperemic eyeballs, lacrimation, depression and anorexia were observed following administration of quinuronium. One rat receiving 5 mg/kg died before termination of the study. When killed 48 h after the first injection, the quinuronium-treated rats had a higher liver weight/body weight ratio compared to the controls. Quinuronium resulted in hepatic centrilobular fatty degeneration, but no depletion of hepatic glutathione (GSH). The present findings suggest that glutathione depletion does not seem to be involved in quinuronium hepatotoxicity.

Two groups of 6 rats each received subcutaneous injections of 2.3 mg/kg or 5.0 mg/kg of quinuronium, respectively, on two consecutive days, while 5 rats injected with physiological saline served as controls. Clinical signs of muscular tremors, jumps, enlarged and hyperemic eyeballs, lacrimation, depression and anorexia were observed following administration of quinuronium. One rat receiving 5 mg/kg died before termination of the study. When killed 48 h after the first injection, the quinuronium-treated rats had a higher liver weight/body weight ratio compared to the controls. Quinuronium resulted in hepatic centrilobular fatty degeneration, but no depletion of hepatic glutathione (GSH). The present findings suggest that glutathione depletion does not seem to be involved in quinuronium hepatotoxicity.

Two groups of 6 rats each received subcutaneous injections of 2.3 mg/kg or 5.0 mg/kg of quinuronium, respectively, on two consecutive days, while 5 rats injected with physiological saline served as controls. Clinical signs of muscular tremors, jumps, enlarged and hyperemic eyeballs, lacrimation, depression and anorexia were observed following administration of quinuronium. One rat receiving 5 mg/kg died before termination of the study. When killed 48 h after the first injection, the quinuronium-treated rats had a higher liver weight/body weight ratio compared to the controls. Quinuronium resulted in hepatic centrilobular fatty degeneration, but no depletion of hepatic glutathione (GSH). The present findings suggest that glutathione depletion does not seem to be involved in quinuronium hepatotoxicity.

Two groups of 6 rats each received subcutaneous injections of 2.3 mg/kg or 5.0 mg/kg of quinuronium, respectively, on two consecutive days, while 5 rats injected with physiological saline served as controls. Clinical signs of muscular tremors, jumps, enlarged and hyperemic eyeballs, lacrimation, depression and anorexia were observed following administration of quinuronium. One rat receiving 5 mg/kg died before termination of the study. When killed 48 h after the first injection, the quinuronium-treated rats had a higher liver weight/body weight ratio compared to the controls. Quinuronium resulted in hepatic centrilobular fatty degeneration, but no depletion of hepatic glutathione (GSH). The present findings suggest that glutathione depletion does not seem to be involved in quinuronium hepatotoxicity.